ArticleBiochemistry2019
Exclusivity and Compensation in NFκB Dimer Distributions and IκB Inhibition.
Article in Biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Frustration in physiology and molecular medicine.Molecular aspects of medicine · 2025Review
- The Role of Redox Environment in Tumors.Current medicinal chemistry · 2025Review
- NF-κB role on tumor proliferation, migration, invasion and immune escape.Cancer gene therapy · 2024Review
- Biophysical characterization of RelA-p52 NF-κB dimer-A link between the canonical and the non-canonical NF-κB pathway.Protein science : a publication of the Protein Society · 2024Article
- Peroxisome Proliferator-Activated Receptor δ Suppresses the Cytotoxicity of CD8+ T Cells by Inhibiting RelA DNA-Binding Activity.Cancer research communications · 2024Article
- The multifunctional role of intrinsic disorder in NF-κB signaling.Biochemical Society transactions · 2023Review
- The Recent Research Progress of NF-κB Signaling on the Proliferation, Migration, Invasion, Immune Escape and Drug Resistance of Glioblastoma.International journal of molecular sciences · 2023Review
- Site-specific incorporation of biophysical probes into NF-ĸB with non-canonical amino acids.Methods (San Diego, Calif.) · 2023Article
- Expression of IkappaB Family in the Ovine Liver during Early Pregnancy.Animals : an open access journal from MDPI · 2023Article
- The NFκB signaling system in the generation of B-cell subsets: from germinal center B cells to memory B cells and plasma cells.Frontiers in immunology · 2023Review
- SUMOylation of Dorsal attenuates Toll/NF-κB signaling.Genetics · 2022Article
- NF-κB, a culprit of both inflamm-ageing and declining immunity?Immunity & ageing : I & A · 2022Review
- Atypical IκB Bcl3 enhances the generation of the NF-κB p52 homodimer.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The NFκB transcription factor family members RelA, p50, and cRel form homo- and heterodimers that are inhibited by IκBα, IκBβ, and IκBε. These NFκB family members have diverse biological functions, and their expression profiles differ, leading to different concentrations in different tissue types. Here we present definitive biophysical measurements of the NFκB dimer affinities and inhibitor affinities to better understand dimer exchange and how the presence of inhibitors may alter the equilibrium concentrations of NFκB dimers in the cellular context. Fluorescence anisotropy binding experiments were performed at low concentrations to mimic intracellular concentrations. We report binding affinities much stronger than those that had been previously reported by non-equilibrium gel shift and analytical ultracentrifugation assays. The results reveal a wide range of NFκB dimer affinities and a strong preference of each IκB for a small subset of NFκB dimers. Once the preferred IκB is bound, dimer exchange no longer occurs over a period of days. A mathematical model of the cellular distribution of these canonical NFκB transcription factors based on the revised binding affinities recapitulates intracellular observations and provides simple, precise explanations for observed cellular phenomena.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.